7 results match your criteria: "From the Center for Molecular Medicine and.[Affiliation]"
Letter by Hüttemann et al Regarding Article, "Ndufs2, a Core Subunit of Mitochondrial Complex I, Is Essential for Acute Oxygen-Sensing and Hypoxic Pulmonary Vasoconstriction".
Circ Res
September 2019
From the Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, MI (M.H., L.I.G.).
The cellular stress proteins CHCHD10 and MNRR1 (CHCHD2): Partners in mitochondrial and nuclear function and dysfunction.
J Biol Chem
April 2018
From the Center for Molecular Medicine and Genetics, Wayne State University, Detroit, Michigan 48201.
Coiled-coil-helix-coiled-coil-helix domain-containing 10 (CHCHD10) and CHCHD2 (MNRR1) are homologous proteins with 58% sequence identity and belong to the twin CXC family of proteins that mediate cellular stress responses. Despite the identification of several neurodegeneration-associated mutations in the gene, few studies have assessed its physiological role. Here, we investigated CHCHD10's function as a regulator of oxidative phosphorylation in the mitochondria and the nucleus.
View Article and Find Full Text PDFToll-like Receptor (TLR) Signaling Interacts with CREBH to Modulate High-density Lipoprotein (HDL) in Response to Bacterial Endotoxin.
J Biol Chem
October 2016
Department of Immunology and Microbiology,
Article Synopsis
- - Bacterial endotoxin triggers inflammation and metabolic responses in the body, and this study explores how a liver-specific transcription factor, CREBH, helps protect the liver from damage caused by lipopolysaccharide (LPS), a component of bacterial endotoxin.
- - CREBH is activated in the liver through a signaling pathway that involves toll-like receptor (TLR) and MyD88, and it interacts with TRAF6, an important mediator in this signaling process.
- - The activation of CREBH leads to the production of the Apolipoprotein A4 (ApoA4) gene, which is crucial for increasing high-density lipoprotein (HDL) levels; a lack of CREBH results in lower HDL
Mammalian cytochrome c (Cytc) plays a key role in cellular life and death decisions, functioning as an electron carrier in the electron transport chain and as a trigger of apoptosis when released from the mitochondria. However, its regulation is not well understood. We show that the major fraction of Cytc isolated from kidneys is phosphorylated on Thr, leading to a partial inhibition of respiration in the reaction with cytochrome c oxidase.
View Article and Find Full Text PDFAlthough exercise is linked with improved health, the specific molecular mechanisms underlying its various benefits require further clarification. Here we report that exercise increases the nuclear localization and activity of p53 by acutely down-regulating coiled-coil-helix-coiled-coil-helix domain 4 (CHCHD4), a carrier protein that mediates p53 import into the mitochondria. This response to exercise is lost in transgenic mice with constitutive expression of CHCHD4.
View Article and Find Full Text PDFHuman pluripotent stem cells have a novel mismatch repair-dependent damage response.
J Biol Chem
August 2014
From the Center for Molecular Medicine and Neag Comprehensive Cancer Center, University of Connecticut Health Center, Farmington, Connecticut 06030-3101
Human pluripotent stem cells (PSCs) are presumed to have robust DNA repair pathways to ensure genome stability. PSCs likely need to protect against mutations that would otherwise be propagated throughout all tissues of the developing embryo. How these cells respond to genotoxic stress has only recently begun to be investigated.
View Article and Find Full Text PDFOsteoclast differentiation is regulated by transcriptional, post-transcriptional, and post-translational mechanisms. MicroRNAs are fundamental post-transcriptional regulators of gene expression. The function of the miR-29 (a/b/c) family in cells of the osteoclast lineage is not well understood.
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